We will investigate the chemical regulation of breathing in normal and obese volunteers, with healthy lungs, while the subjects are awake during slow-wave (SW) and rapid eye movement (REM) sleep. We will compare in each of these states: 1) hypoxic and hypercapnic sensitivity; 2) changes in the relative influence of hypoxia and hypercapnia on breathing; and 3) the distribution of respiratory output to pharyngeal and to inspiratory skeletal muscles (external intercostal and diaphragm). Hypoxia and hypercapnia will be produced awake and in each sleep state by steady state and rebreathing methods. Since airway resistance and chest wall mechanics change during sleep, respiratory efferent activity will be assessed from recordings of respiratory and pharyngeal muscle EMG as well as by measurements of ventilation; and a rib cage and abdominal movement. We will also examine the effects of resistive and elastic loads on breathing and the effects of mechanical and chemcal stimuli in causing arousal or switches in sleep stage. The data obtained will be used to amplify a mathematical model of the chemical control of breathing and to test the following hypotheses: 1) that depressed chemosensitivity in the awake state is associated with hypoventilation and blunted responses to chemical stimulation occur during sleep; 2) that recurrent central sleep apneas appear whenever peripheral chemoreceptor input dominates the activity of the central respiratory neurons and causes instability in chemical control; 3) that obstructive apnea is promoted by unequal effects of chemical drive on the electrical activity of pharyngeal and inspiratory skeletal muscles; 4) that instability in chemical control and the resulting occurrence of central sleep apnea increases the frequency of obstructive apnea, and the conversely obstructive apneas may increase the frequency of central apneas; 5) that irregularities in breathing are related to the effects of mechanical and chemical stimuli on sleep state; and 6) that metabolic alkalosis and acidosis sufficient to shift CO2 response lines will also alter the occurrence of central and obstructive sleep apneas.